Wk 6 Assgn Abraham M(meena) Pathophysiology.docx - Asthma Meena Abraham Walden University Advanced Pathophysiology NURS 6501N Asthma Asthma is a chronic

Wk 6 Assgn Abraham M(meena) Pathophysiology.docx - Asthma...

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Asthma Meena Abraham Walden University Advanced Pathophysiology NURS 6501N 10/06/19
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Asthma Asthma is a chronic inflammatory disease of the mucosal lining of the bronchus. Bronchus becomes more swollen and the muscles around the airways becomes tighten when something triggers the symptoms which causes difficulty in the movement of the air in and out of the lungs. As a result, the symptoms such as coughing, wheezing, shortness of breath or chest tightness can be seen in patients with Asthma AAAA, n. d) The purpose of this paper is to describe the pathophysiology of both acute and chronic asthma including the arterial blood gas patterns and to explain the impact of behaviors on the exacerbation of Asthma and the diagnosis/treatment of the case. Mind maps of both acute and chronic asthma is included at the end of the paper. Pathophysiological Mechanism of Chronic and Acute Asthma Almost 6.8 million adults and 18.7 million children are affected by Asthma in United states. It is a chronic inflammatory response of the bronchial mucosa. There are immediate and adaptive response in individuals when they are exposed to antigen. The pathophysiology of Asthmatic attack is explained by Huether and McCance (2017) are as follows. When a person is exposed to an antigen it enters the bronchial mucosa and produce an early asthmatic response by activating the dendritic cells which presents antigen to T helper cells. T helper cells differentiate in to Th 2 cells and release cytokines and interleukins which activate B lymphocytes (plasma cells) and eosinophils. Plasma cells produce antigen specific IgE (Immunoglobulins) which binds to the surface of the mast cells and causes mast cell degranulation. It releases inflammatory mediators such as histamine, bradykinin, leukotrienes, and platelet activating factor, and interleukins. These mediators are the reason for vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchospasm) and mucus secretion from
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mucosal goblet cells with narrowing of the airways and obstruction to the airflow. Moreover, the eosinophils cause direct tissue injury and increased bronchial hyperresponsiveness due to release of toxic neuropeptides. After 4-8 hours of early asthmatic response, the late asthmatic response starts. The chemotactic mediators during early response causes cellular infiltration of eosinophils, neutrophils and lymphocytes which further causes a latent release of inflammatory mediators causing bronchospasm, edema, and mucus secretion with airflow obstruction. Leukotrienes causes prolonged smooth muscle contraction and eosinophils causes fibroblast proliferation and airway scarring. As a result of the damage to the ciliated epithelial cells, impaired function of mucociliary cells, accumulation of cellular debris and mucus and formation of mucosal plugs in the airways occurs. If this condition goes untreated a long-term airway damage called airway remodeling occurs and the condition is irreversible. The airway remodeling includes subepithelial fibrosis, and smooth muscle hypertrophy of the airways.
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